摘要
目的观察再发性低血糖后脑内葡萄糖转运蛋白1(glucose transporter 1,GLUT1)及葡萄糖转运蛋白3(GLUT3)表达的变化,从而探讨无症状低血糖的发生机制。方法将80只15日龄野生型小鼠随机分为正常对照组及低血糖组,每组40只。低血糖组给予正规胰岛素腹腔注射3次,每次剂量为5U/kg,对照组注射等体积生理盐水。两组分别在最后1次注射后12、24、48及72 h处死小鼠取脑组织(每组每时间点10只),应用免疫组化方法观察小鼠脑内GLUT1及GLUT3表达的变化。结果低血糖后脑内微血管上GLUT1表达有增加趋势,皮质增加高于海马,72 h皮质GLUT1表达显著高于对照组;低血糖后48、72 h皮质及海马GLUT3表达均显著高于相应对照组。结论再发性低血糖后脑内GLUT1及GLUT3适应性增高,这种适应既能节省神经元的能量代谢,但也能削减神经元对低血糖的反应。
Objective To investigate the role of brain glucose transporter 1 （GLUT1） and glucose transporter 3 （GLUT3） in cerebral adaptation to recurrent hypoglycemia, and clarify the mechanisms of unawareness hypoglycemia. Methods Eighty mice were randomly assigned into control group （ n = 40） and hypoglycemia group （ n = 40）. The mice in hypoglycemia group were intraperitoneally injected with insulin three times at the dose of 5U/kg, and were killed at 12, 24, 48 and 72 h after the third injection. Mice in control group were injected with NS, and were killed at the same time. GLUT1 and GLUT3 expressions in mice brain were determined by immunohistochemical method. Results Following three times hypoglycemia, microvascular GLUT1 tended to increased variably, but only the increment of cortex at 72 h after hypoglycemia was significant comparing to control group. In contrast, at 48 h and 72 h after hypoglycemia, the expression of GLUT3 protein in both cortex and hippocampus increased significantly comparing to those in control group. Conclusion These data suggest that neuronal glucose transport protein expression can adapt to recurrent hypoglycemia. This adaptation may spare neuronal energy metabolism but could dampen neuronal signaling of glucose deprivation.
出处
《中国小儿急救医学》
CAS
2006年第3期253-255,共3页
Chinese Pediatric Emergency Medicine
基金
教育部留学回国人员科研启动基金(教外司留[2004]527号)
关键词
葡萄糖转运蛋白
低血糖症
脑
幼鼠
Glucose transporter
Hypoglycemia
Brain
Young mouse
